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How Breast Cancer Cells Evade Anti-Cancer Drugs

Estrogen is a hormone present in both men and women. But it is present in much higher levels in women of reproductive age. It promotes the development of breasts in them. In 70 percent of cases, this hormone is responsible for the survival and growth of malignant cancer tumour cells in this organ. It is for this reason that the most common treatment technique of breast cancer is giving drugs which inhibits the functions of this hormone, like Tamoxifen. But in 30 percent cases, there is a resistance to this therapy. Scientists have been trying hard to understand the mechanism behind the resistance faced by Tamoxifen drug from cancer cells. Researchers from the University of Geneva have discovered the answer very recently. The results of the findings are published in the April edition of the journal Genes & Development. This article tries to gain further insight on this topic.

Knowledge Gained from Research:

The malignant cancer cells have receptors of the hormone estrogen in their nucleus.

This is the reason why in two-third cases of breast cancer, estrogen plays a key role in the progression of the disease.

This hormone changes the chemical instructions called genes which regulate the functioning of the cancer cells in a manner that they can survive inside the body.

The drug Tamoxifen tries to disturb the communication between the hormone estrogen and its receptors inside the nucleus in order to inhibit the tumour growth, partially.

The research study found out that there are other receptors which are also activated by their signalling molecules, like the ERalpha receptor.

Researchers focused their attention on understanding the role played by ERalpha receptor in stimulating cancer cells.

They identified a molecule called Cyclic AMP which is a secondary messenger.

Secondary messengers are required to transmit information between the interior and exterior of cells.

Hormones and neurotransmitters seek the help of secondary messengers when they fail to transmit information to the cells.

The ERalpha receptor is found to be activated by the Cyclic AMP molecule in the absence of Estrogen hormone to promote continuous growth of malignant cancer tumour in the breasts.

This leads to a series of chemical reactions forming a protein called CARM 1.

CARM 1 protein immediately after its formation, gets attached with ERalpha receptor, activating it once again.

In this way, the drug Tamoxifen continuously faces opposition from cancer cells even in the absence of estrogen hormone.

Further research is targeted towards developing drugs which can inhibit the interaction between ERalpha receptor and CARM 1 protein.